The long-term goal is to understand the genetic control of animal development in a simple model system. The experimental approach applies genetic, microscopic, ultrastructural and biochemical methods to a detailed analysis of a particular "developmental switch" in the life cycle of C. elegans, the formation of dauer larvae. The dauer larva is formed when food is scarce; it neither feeds nor grows and it possesses a unique, relatively impermeable cuticle. When dauer larvae encounter food, they molt and resume development. Some mutants affected in entry into, and exit from, the dauer stage exhibit sensory defects correlated with ultrastructural abnormalities in specific neurons. Mutant genes controlling the ability to form dauers interact in a way which allows them to be ordered in a pathway. We have proposed that the genetic pathway corresponds to neural processing of environmental stimuli involving reception of an environmental signal, and conversion of that signal into a neuroendocrine response. Two types of mutant have been characterized: "constitutive" mutants which produce dauer larvae even when food is abundant, and "defective" mutants which do not produce dauer larvae. Genetic analysis of a complete catalogue of single-step mutants will be used to determine the genetic structure of the entire developmental sequence by assigning mutant genes to positions in "signal" and "process" pathways. At present, temperature-sensitive mutants are being used to determine at which stages in development particular gene activities are required. Normal entry into, and exit from, the dauer stage will be characterized more fully by determining: (1) the timing of commitment to the pathway, (2) the nature of the environmental cues, (3) what neurotransmitters may be utilized, and (4) what role cyclic nucleotides or steroids may play in hormonal controls. Internal points in the genetic pathway will be correlated with cellular abnormalities by ultrastructural analysis. Parallel experiments using laser microsurgery will identify neurons required for normal signalling in wild-type animals. This work will provide a model for genetic and physiological controls of the development and sensory behavior of a simple animal.